Nonsteroidal anti-inflammatory drugs (NSAIDs) block prostaglandin and prostacyclin biosynthesis via their inhibition of cyclooxygenase (COX) enzymes. By inhibiting COX-1, aspirin reduces thromboxane production, and this leads to its antiplatelet effect. By more effectively inhibiting COX-2, other NSAIDs have relatively greater anti-inflammatory, antipyretic, and analgesic effects. The adverse effect profile of nonselective NSAIDs includes bleeding, particularly gastrointestinal bleeding, which is thought to result from gastric irritation, antiplatelet effects, and the loss of prostaglandin-mediated mucosal repair.1 Selective inhibitors of COX-2 were developed with the hope they would have fewer gastrointestinal adverse effects and would be highly effective against chronic inflammatory states, such as arthritis.